Huntington's Disease (HD) is an autosomal dominant neurodegenerative disorder caused by CAG trinucleotide repeat expansions in the HTT (huntingtin) gene. The disease manifests with progressive motor dysfunction, cognitive decline, and psychiatric disturbances, typically beginning in mid-adulthood. This article explores the genetic basis of HD, its pathological features, and advancements in therapeutic approaches, including gene-silencing strategies and symptom-targeted treatments. Ongoing research into molecular mechanisms and clinical interventions holds promise for improved management and potential disease-modifying therapies.